Case Presentation:

A 37‐year‐old HIV‐positive obese man on highly active antiretroviral therapy (HAART) was admitted with progressive dyspnea and right upper quadrant pain without tenderness to palpation. His chest x‐ray revealed a right pleural effusion. His initial blood tests showed a normal white blood cell count, lactate of 8.1 mmol/L, high anion‐gap metabolic acidosis, creatinine of 1.6 mg/dL, absolute CD4 count of 441 cells/μL, and hemoglobin of 11.7 g/dL. He was hemodynamically stable, requiring minimal oxygen support, and was started on empiric broad‐spectrum antibiotics. HAART was discontinued on admission because of mildly elevated liver enzymes. Further studies included a CT of the abdomen that revealed infiltrative soft‐tissue density and inflammatory changes in the right perinephric area. Pancul‐tures and autoimmune studies were negative. Viral hepatitis serology was also negative. Pleural fluid cytology unveiled non‐Hodgkin lymphoma (NHL). During the first 12 hours of hospitalization, he developed acute kidney injury with microscopic evidence of granular casts and hyperuricemia without biochemical markers of tumor lysis syndrome. He was started on allopurinol and intravenous isotonic fluids with sodium bicarbonate. Bone marrow biopsy confirmed the diagnosis of NHL (phenotype CD45, CD5, and CD19 positive) and the patient was evaluated for initiation of chemotherapy. Unfortunately, his lactic acidosis (LA) and kidney and liver dysfunction worsened over the next hours (Table 1) triggering a fatal pulseless cardiac arrest. Autopsy confirmed NHL involving axillary, abdominal, and mediastinal lymph nodes; pericardium; pleura; right kidney forming subcapsular nodules that invaded into the parenchyma; right perinephric Gerota's fascia; and pericolic and mesenteric adipose tissue.

TABLE 1 Laboratory Features


Type B LA is infrequently associated with hematologic malignancies, but its development is a concerning oncologic emergency that carries devastating consequences, with mortality rates in the range of 95%. It can occur in the absence of a recognizable impairment in systemic oxygen delivery, resulting from abnormal oxidative phosphorylation. It is hypothesized that increased glycolysis in cancer cells, through insulin‐like growth factor‐I and overexpression of mitochondrial hexoki‐nases, is implicated in lactic acid generation despite normal tissue oxygenation. The presence of hyperlactatemia arises when the lactate burden enters the systemic circulation and exceeds the capacity of muscle uptake and hepatic and renal clearance.


Our case highlights the severe metabolic derangements of type B LA and the importance of prompt recognition and diagnosis. Although intravenous bicarbonate and dialysis could be temporary effective strategies, early initiation of chemotherapy is the best therapeutic intervention.


G. Hurst ‐ none; J. Neyra ‐ none